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pubmed-article:2150599pubmed:abstractTextThe Mos protein is a serine/threonine protein kinase that is likely to be a part of signal transduction pathways that regulate cell growth. We show here that expression of the v-Mos protein leads to a transient transcriptional activation of the c-fos and the c-jun proto-oncogenes in NIH 3T3 cells. Different cis-acting promoter elements are responsible for this effect. In the c-fos promoter the dyad symmetry element (DSE, also known as serum response element, SRE) is sufficient to confer responsiveness to the v-Mos protein. In the c-jun promoter the 12-0-tetradecanoyl-phorbol-13-acetate (TPA) response element (TRE) mediates this effect. Various Mos mutants with decreased transforming activity have diminished trans-acting activity on the c-fos and c-jun promoters. These results suggest that the highly transforming v-Mos protein exerts at least some of its effects through the induction of expression of the c-fos and c-jun protooncogenes.lld:pubmed
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pubmed-article:2150599pubmed:dateRevised2008-11-21lld:pubmed
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pubmed-article:2150599pubmed:articleTitleDifferent promoter elements are required for the induced expression of c-fos and c-jun proto-oncogenes by the v-mos oncogene product.lld:pubmed
pubmed-article:2150599pubmed:affiliationDepartment of Medicine, University of California, San Diego, La Jolla 92093.lld:pubmed
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